Hypertonic/hyperoncotic fluid resuscitation after hemorrhagic shock in dogs.

We compared canine systemic and cerebral hemodynamics after resuscitation from hemorrhagic shock with 4 mL/kg (a volume approximating 12% of shed blood volume) of 7.2% saline (HS; 1233 mEq/L sodium), 20% hydroxyethyl starch (HES) in 0.8% saline, or a combination fluid consisting of 20% hydroxyethyl starch in 7.2% saline (HS/HES). Eighteen endotracheally intubated mongrel dogs (18-24 kg) were ventilated to maintain normocarbia with 0.5% halothane in nitrous oxide and oxygen (60:40). After a 30-min period of hemorrhagic shock (mean arterial blood pressure = 40 mm Hg), extending from time T0 to T30, animals received one of three randomly assigned intravenous resuscitation fluids: HS, HES, or HS/HES. Data were collected at baseline, at the beginning and end of the shock period (T0 and T30), immediately after fluid infusion (T35), and at 60-min intervals for 2 h (T95, T155). After resuscitation, mean arterial blood pressure and cardiac output increased similarly in all groups, but failed to return to baseline. Intracranial pressure decreased during shock and increased slightly, immediately after resuscitation in all groups. During shock, cerebral blood flow (cerebral venous outflow method) declined in all groups. After resuscitation, cerebral blood flow increased, exceeding baseline in the HS and HS/HES groups but remaining low in the HES group (P less than 0.05 HS vs HES at T35). We conclude that small-volume resuscitation (4 mL/kg) with HS, HS/HES, or HES does not effectively restore or sustain systemic hemodynamics in hemorrhaged dogs. In dogs without intracranial pathology, the effects on cerebral hemodynamics are also comparable, except for transiently greater cerebral blood flow in the HS group in comparison with the HES group.     

Effects of hypertonic saline versus lactated Ringer's solution on cerebral oxygen transport during resuscitation from hemorrhagic shock

Hypertonic saline successfully restores systemic hemodynamics in dogs and humans with severe hemorrhagic shock and, in contrast to lactated Ringer's solution, does not increase intracranial pressure (ICP). This study compares cerebral oxygen delivery in 12 dogs subjected to hemorrhagic shock by the rapid removal of blood (mean arterial pressure of 40 mm Hg maintained for 30 minutes), and then resuscitated with lactated Ringer's solution (six dogs) or 7.5% saline solution (six dogs) to restore systolic arterial pressure. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and systolic blood pressure while decreasing mean and diastolic arterial pressure and systemic vascular resistance. The ICP was significantly lower after resuscitation in the hypertonic saline group (p less than 0.05), but cerebral blood flow, which had decreased during shock, was not restored by either fluid, and cerebral oxygen transport fell further secondary to a hemodilutional reduction of hemoglobin. Although hypertonic saline may improve systemic hemodynamics and maintain a low ICP during resuscitation, it fails, as does Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.     

Early hemodynamic and renal effects of hemorrhagic shock resuscitation with lactated Ringer's solution, hydroxyethyl starch, and hypertonic saline with or without 6% dextran-70

BACKGROUND: Considering the renal effects of fluid resuscitation in hemorrhaged patients, the choice of fluid has been a source of controversy. In a model of hemorrhagic shock, we studied the early hemodynamic and renal effects of fluid resuscitation with lactated Ringer's (LR), 6% hydroxyethyl starch (HES), and 7.5% hypertonic saline (HS) with or without 6% dextran-70 (HSD). MATERIALS AND METHODS: Forty-eight dogs were anesthetized and submitted to splenectomy. An estimated 40% blood volume was removed to maintain mean arterial pressure (MAP) at 40 mm Hg for 30 min. The dogs were divided into four groups: LR, in a 3:1 ratio to removed blood volume; HS, 6 mL kg(-1); HSD, 6 mL kg(-1); and HES in a 1:1 ratio to removed blood volume. Hemodynamics and renal function were studied during shock and 5, 60, and 120 min after fluid replacement. RESULTS: Shock treatment increased MAP similarly in all groups. At 5 min, cardiac filling pressures and cardiac performance indexes were higher for LR and HES but, after 120 min, there were no differences among groups. Renal blood flow and glomerular filtration rate (GFR) were higher in LR at 60 min but GFR returned to baseline values in all groups at 120 min. Diuresis was higher for LR at 5 min and for LR and HES at 60 min. There were no differences among groups in renal variables 120 min after treatment. CONCLUSIONS: Despite the immediate differences in hemodynamic responses, the low-volume resuscitation fluids, HS and HSD, are equally effective to LR and HES in restoring renal performance 120 min after hemorrhagic shock treatment.     

The early systemic and gastrointestinal oxygenation effects of hemorrhagic shock resuscitation with hypertonic saline and hypertonic saline 6% dextran-70: a comparative study in dogs

The smaller volemic state from hypertonic (7.5%) saline (HS) solution administration in hemorrhagic shock can determine lesser systemic oxygen delivery and tissue oxygenation than conventional plasma expanders. In a model of hemorrhagic shock in dogs, we studied the systemic and gastrointestinal oxygenation effects of HS and hyperoncotic (6%) dextran-70 in combination with HS (HSD) solutions in comparison with lactated Ringer's (LR) and (6%) hydroxyethyl starch (HES) solutions. Forty-eight mongrel dogs were anesthetized, mechanically ventilated, and subjected to splenectomy. A gastric air tonometer was placed in the stomach for intramucosal gastric CO(2) (Pgco(2)) determination and for the calculation of intramucosal pH (pHi): The dogs were hemorrhaged (42% of blood volume) to hold mean arterial blood pressure at 40-50 mm Hg over 30 min and were then resuscitated with LR (n = 12) in a 3:1 relation to removed blood volume; HS (n = 12), 6 mL/kg; HSD (n = 12), 6 mL/kg; and HES (mean molecular weight, 200 kDa; degree of substitution, 0.5) (n = 12) in a 1:1 relation to the removed blood volume. Hemodynamic, systemic, and gastric oxygenation variables were measured at baseline, after 30 min of hemorrhage, and 5, 60, and 120 min after intravascular fluid resuscitation. After fluid resuscitation, HS showed significantly lower arterial pH and mixed venous Po(2) and higher systemic oxygen uptake index and systemic oxygenation extraction than LR and HES (P < 0.05), whereas HSD showed significantly lower arterial pH than LR and HES (P < 0.05). Only HS and HSD did not return arterial pH and pHi to control levels (P < 0.05). In conclusion, all solutions improved systemic and gastrointestinal oxygenation after hemorrhagic shock in dogs. However, the HS solution showed the worst response in comparison to LR and HES solutions in relation to systemic oxygenation, whereas HSD showed intermediate values. HS and HSD solutions did not return regional oxygenation to control values.     

Regional cerebral blood flow following resuscitation from hemorrhagic shock with hypertonic saline. Influence of a subdural mass.

After severe hemorrhage, hypertonic saline restores systemic hemodynamics and decreases intracranial pressure (ICP), but its effects on regional cerebral blood flow (rCBF) when used for resuscitation of experimental animals with combined shock and intracranial hypertension have not been reported. We compared rCBF changes (by radiolabeled microsphere technique) after resuscitation from hemorrhage with either 0.8 or 7.2% saline in animals with and without a right hemispheric subdural mass. We studied 24 mongrel dogs anesthetized with 0.5% halothane and 60% nitrous oxide. In group 1 (n = 12), hemorrhage reduced mean arterial pressure (MAP) to 45 mmHg for 30 min. In group 2 (n = 12), ICP was increased and maintained constant at 15 mmHg, whereas hemorrhage reduced MAP to 55 mmHg for 30 min (cerebral perfusion pressure [CPP] approximately 40 mmHg in each group). After the 30-min shock period, 6 animals in each group received one of two randomly assigned resuscitation fluids over a 5-min interval: 1) 7.2% hypertonic saline (HS; sodium 1,232 mEq.l-1, volume 6.0 ml.kg-1); or 2) 0.8% isotonic saline (SAL; sodium 137 mEq.l-1, volume 54 ml.kg-1). Once fluid resuscitation began, ICP was permitted to vary independently in both groups. Data were collected at baseline (before subdural balloon inflation in group 2), midway through the shock interval (T15), immediately after fluid infusion (T35), and 60 and 90 min later (T95, T155). In groups 1 and 2, ICP was significantly less in animals resuscitated with HS compared to those receiving SAL (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

The synergistic effects of pentoxifylline on systemic and regional perfusion after hemorrhage and hypertonic resuscitation

Small volumes of hypertonic saline solution ([HS] 7.5% NaCl) produce systemic and microcirculatory benefits in hemorrhaged animals. Pentoxifylline (PTX) has beneficial effects when administrated after hemorrhagic shock. We tested the hypothesis that the combination of HS and PTX in the initial treatment of hemorrhagic shock provides synergistic hemodynamic benefits. Twenty-four dogs were bled to a target arterial blood pressure of 40 mm Hg and randomized into 3 groups: lactated Ringer's solution (33 mL/kg; n = 6); HS (7.5% NaCl 4 mL/kg; n = 9); and HS+PTX (7.5% NaCl 4 mL/kg + PTX 15 mg/kg; n = 9). Systemic hemodynamics were measured by Swan-Ganz and arterial catheters. Gastric mucosal-arterial Pco2 gradient (D(g-a)Pco2; gas tonometry), portal vein blood flow (ultrasonic flowprobe), and systemic and regional O2-derived variables were also evaluated. HS induced a partial increase in mean arterial blood pressure, cardiac output, and portal vein blood flow. In the HS+PTX group, we observed a significant, but transitory, increase in systemic oxygen delivery (180 +/- 17 versus 141 +/- 13 mL/min) in comparison to HS alone. PTX infusion during hypertonic resuscitation promoted a significant reduction in D(g-a)Pco2 (41.8 +/- 4.8 to 25.7 +/- 3.9 mm Hg) when compared with isolated HS infusion (48.2 +/- 6.4 to 39.4 +/- 5.5 mm Hg). We conclude that PTX as an adjunct drug during hypertonic resuscitation improves cardiovascular performance and gastric mucosal oxygenation.     

Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion

We compared intracranial pressure (ICP) and cerebral blood flow (CBF) in dogs after inflating a subdural intracranial balloon to increase ICP to 20 mm Hg, inducing hemorrhagic shock (mean arterial pressure [MAP] of 55 mm Hg), and infusing a single bolus of fluid consisting of either 54 mL/kg of 0.8% saline (SAL), 6 mL/kg of 7.2% hypertonic saline (HS), 20% hydroxyethyl starch (HES) in 0.8% SAL, or a combination fluid (HS/HES) containing 20% HES in 7.2% saline. Twenty-six dogs were ventilated with 0.5% halothane in N2O and O2 (60:40 ratio). As ICP was maintained at 20 mm Hg, rapid hemorrhage reduced MAP to 55 mm Hg (time interval of zero [T0]) which was maintained at that level for 30 minutes (until T30). Subsequently, over a 5-minute interval (T30-T35), one of the four randomly assigned resuscitation fluids was infused. Data were collected at baseline; after subdural balloon inflation; at T0, T30, T35, and 30-minute intervals thereafter for 2 hours (T65, T95, T125, and T155). CBF and ICP were compared using repeat-measure ANOVA. Cerebral blood flow was greater at T35 in the HS and HS/HES groups than in the HES group (P = .025). In the SAL group, ICP increased significantly from T0 to T35, remaining unchanged thereafter. At T35, ICP in the HS group was significantly lower than in the SAL group (P < .05) but subsequently increased. ICP in the HS/HES group exceeded that in all other groups at T95 and T125 (P < .05). After a severe reduction in cerebral perfusion pressure (CPP), HS solutions (both HS and HS/HES) were associated with a delayed rise in ICP and did not improve global forebrain CBF in comparison with conventional saline solutions.     

不同液体容量复苏对失血性休克犬血管外肺水的影响

目的 评价不同液体容量复苏对失血性休克犬血管外肺水的影响。方法 杂种犬32只,雌雄不拘,随机分为4组：NS组、HES组、HS组和HHS组,每组8只,股动脉放血建立失血性休克模型后,各组分别静脉输注容积相当于3倍失血量的生理盐水、失血量等容积的6%羟乙基淀粉130/0．4溶液、7．5%氯化钠溶液6 ml/kg及7．5%氯化钠-6%羟乙基淀粉130/0．4溶液6 ml/kg行容量复苏。经右颈内静脉持续监测中心静脉压、右股动脉置入PiCCO导管监测平均动脉压、心脏指数、每搏输出量、体循环阻力指数、血管外肺水指数及全心舒张末期容量指数,记录放血之前（基础值）、失血性休克模型成功即刻、容量复苏开始后5、30、60、120及180min的上述指标。结果 （1）各组在失血性休克的早期复苏中均可改善血液动力学,HES组、HHS组、HS组和NS组血液动力学改善持续时间依次缩短;（2）复苏早期HS组与HHS组血管外肺水无增加,NS组明显增加,而HES组下降。结论 （1） 7．5%氯化钠溶液与7．5%氯化钠-6%羟乙基淀粉130/0．4溶液小容量液体复苏可有效恢复犬失血性休克早期血液动力学的稳定,且不增加休克后血管外肺水,7．5%氯化钠-6%羟乙基淀粉130/0．4溶液效果较好;（2）6%羟乙基淀粉130/0．4溶液用于犬失血性休克早期复苏不仅可以改善血液动力学,而且能防止复苏后肺水肿。     

Heterogeneous microcirculation in the rat small intestine during hemorrhagic shock: quantification of the effects of hypertonic-hyperoncotic resuscitation

PURPOSE: In the event of a spatial or temporal microvascular perfusion heterogeneity conventional methods are often inadequate to describe the microcirculatory changes. Our aim was to use a new formula to characterize and compare the microcirculatory reactions in the mucosa and longitudinal muscle of the rat small intestine in response to hypertonic/hyperoncotic and normotonic resuscitation strategies. METHODS: Intravital videomicroscopy with an orthogonal polarization spectral (OPS) imaging technique was utilized. Microcirculatory variables were recorded during hemorrhagic shock (HS; 50 mm Hg mean arterial pressure for 60 min) and fluid replacement with 0.9% saline or with 7.2% saline containing 10% hydroxyethylstarch 200/0.5 (Osmohes; 4 ml/kg). Due to the temporal perfusion variability, microcirculatory changes were described using the calculation of the average red blood cell velocity (A-RBCV), while the spatial changes were calculated as a function of the size of the perfused capillary network. RESULTS: During HS and the late phase of resuscitation, perfusion was characterized by capillary flow motion (i.e. variability in time) in the villi, and by spatial flow heterogeneity in the longitudinal muscle layer. The approximately 40% decrease in the calculated villus A-RBCV during HS was only partially affected by 0.9% saline, whereas Osmohes completely restored A-RBCV by increasing both the red blood cell velocity and the duration of high-flow periods at the onset of resuscitation in the villi. The approximately 60% reduction in A-RBCV in the muscle layer during HS was not followed by an appreciable recovery in either group, but Osmohes significantly increased A-RBCV in the late resuscitation phase. CONCLUSIONS: The hypertonic/hyperoncotic solution induces a considerable microcirculatory improvement in two distinct layers of the small intestine after HS. This positive effect is related to the amelioration of the intestinal microcirculatory heterogeneity.     

Pentoxifylline but not saralasin restores hepatic blood flow after resuscitation from hemorrhagic shock

After determining that hepatic blood flow remains impaired after resuscitation from hemorrhagic shock, we used the angiotensin II receptor antagonist saralasin and pentoxifylline to investigate their respective effects on hepatic blood flow responses after resuscitation from hemorrhagic shock. Rats were bled to 50% of baseline blood pressure for 60 min and resuscitated with shed blood and an equal volume of lactated Ringer's solution. Saralasin [10 micrograms/kg per min (n = 6)], pentoxifylline [25 mg/kg bolus and 12.5 mg/kg per hr (n = 7)], or saline (n = 11) were started with the onset of resuscitation. Total hepatic blood flow measured by ultrasonic transit time flow meter, effective nutrient hepatic blood flow measured by galactose clearance, mean arterial pressure, and cardiac output were recorded at 15-min intervals for 2 hr after resuscitation. Hemorrhage decreased cardiac output 57% below baseline and decreased total hepatic blood flow 64% below baseline. Resuscitation restored cardiac output to baseline levels in all three groups. Despite restoration of cardiac output, total hepatic and effective hepatic blood flow remained significantly below baseline in the saline control and saralasin groups but was restored to baseline levels in the pentoxifylline group. These data indicate that angiotensin II does not contribute significantly to the hepatic blood flow impairment after resuscitation from hemorrhagic shock. Improvement in flow with pentoxifylline implies that hemorrhage and resuscitation impair hepatic microvascular hemorrheology and that addition of pentoxifylline to standard resuscitation corrects the impairment.     

A comparison of several hypertonic solutions for resuscitation of bled sheep

Small volumes (4 ml/kg) of 2400 mOsm NaCl restore cardiac output and mean arterial pressure to 80% of baseline after hemorrhage (65% of blood volume) in unanesthetized sheep. An equal volume of normal saline is less effective. To identify an optimal hypertonic solution, we screened six 2400 mOsm solutions in 18 randomized experiments in 8 sheep: NaCl, NaHCO3, NaCl/sodium acetate, NaCl/mannitol, NaCl/6% Dextran 70, and glucose. Cardiovascular function, as determined by cardiac output and mean arterial pressure, was restored best with NaCl, NaCl/NaAc, and NaCl/Dex. These three solutions were then evaluated using 18 sheep in 36 experiments. Following a 1-hr baseline period, the sheep were bled to a mean arterial pressure of 50 mm Hg for 2 hr. One of the solutions was then given in a volume of 4 ml/kg over 2 min and the sheep were monitored for 3 hr. Within 3 min of the infusion, cardiac output increased to greater than 100% of baseline for all three solutions. The NaCl-Dex solution sustained a significantly higher cardiac output over the 3-hr observation period than the other solutions. Plasma volume increased for all solutions following infusion. NaCl-Dex maintained plasma volume significantly better than the other solutions. As a further control, an isotonic solution of 6% Dextran 70 in normal saline was studied. It was not as effective as the hypertonic NaCl-Dex in maintaining cardiac output, mean arterial pressure, or plasma volume. Osmolality increased 10% (309 to 326 mOsm/kg H2O), plasma [NA] increased 7% (151 to 161 meq/liter), and plasma [K] decreased from 3.9 to 2.6 meq/liter following the hypertonic infusions. The sheep appeared to tolerate these electrolyte changes well. We conclude that a single bolus infusion of 2400 mOsm NaCl with 6% Dextran 70 best resuscitates sheep that have been subjected to a moderate degree of hemorrhagic shock compared to several other solutions. Its beneficial effects are caused in part by a sustained reestablishment of plasma volume. More studies are needed to document the safety of dextran in the clinical setting of hemorrhagic shock. Small volumes of hypertonic solutions may be valuable in the initial fluid resuscitation of patients in hemorrhagic shock.     

Effects of resuscitation from hemorrhagic shock on cerebral hemodynamics in the presence of an intracranial mass

This study compares intracranial pressure, cerebral blood flow, and cerebral oxygen transport during hemorrhagic shock and following fluid resuscitation with crystalloid or colloid solution in a canine model with an epidural mass lesion. After placement of an epidural balloon, intracranial pressure was increased to 30 mm Hg for 5 minutes and then permitted to vary without further manipulation. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure of 55 mm Hg for 30 minutes. Resuscitation then was performed with intravenous lactated Ringer's solution, 60 ml/kg, or with 6.0% hetastarch, 20 ml/kg. Following both solutions mean arterial pressure and cardiac output were increased and hemoglobin concentration was reduced. Intracranial pressure was significantly lower immediately after resuscitation in the hetastarch group; it then gradually increased so that the difference was much less 1 hour later. Cerebral blood flow decreased during shock and was not restored by either fluid; cerebral oxygen transport fell further with resuscitation in both groups due to hemodilutional reductions in hemoglobin. Although colloid resuscitation improved systemic hemodynamics and maintained lower intracranial pressure, it failed, as did crystalloid resuscitation, to restore cerebral oxygen transport to prehemorrhagic shock levels.     

Head injury and hemorrhagic shock: studies of the blood brain barrier and intracranial pressure after resuscitation with normal saline solution, 3% saline solution, and dextran-40

The effect of fluid resuscitation from hemorrhagic shock on cerebral edema, intracranial pressure (ICP), and blood brain barrier function was investigated in the presence of a simulated head injury. Beagle dogs were anesthetized and ICP was measured via a right subarachnoid bolt while a contralateral epidural balloon was inflated in the left hemicranium to mimic a closed head injury. Forty percent of the dogs' blood was shed and the shock state was maintained for 1 hour. Resuscitation was initiated with shed blood and a volume of either normal saline solution (NS, n = 5), 10% dextran-40 (D-40, n = 6), or hypertonic (3%) saline solution (HS, n = 6) equal to the amount of shed blood. Evans blue solution was infused intravenously, and intravascular volume was then maintained with normal saline solution. Control (n = 5) dogs did not undergo shock, but received equivalent volumes of normal saline solution and Evans blue solution. The dogs were killed after 2 hours of resuscitation, and the brains were removed, weighed, and fixed in formalin. The average intracranial pressure value after epidural balloon inflation was 18.6 +/- 0.80 mm Hg and decreased equally in all groups during the shock period, averaging 10.8 +/- 1.24 mm Hg at the end of the shock period. Fluid resuscitation markedly elevated ICP in the NS and D-40 groups, reaching maximal values of 46.6 +/- 12.11 mm Hg and 45.3 +/- 28.95 mm Hg, respectively. Maximal ICP values in control and HS groups measured 21.8 +/- 1.36 mm Hg and 15.8 +/- 2.04 mm Hg, respectively (p less than 0.25 for HS versus NS control). Wet brain weights were significantly less in the HS group compared with either NS or D-40 groups (p less than 0.05). Coronal sections of fixed HS brains showed deep cortical Evans blue staining on the side of balloon injury. Therefore, in the presence of an intracranial mass lesion, resuscitation with hypertonic (3%) saline solution is accompanied by lower ICP values and less cerebral edema than is isotonic saline or colloid resuscitation. Blood brain barrier function is not restored by hypertonic saline solution resuscitation.     

Initial management of severe hemorrhage with an oxygen-carrying hypertonic saline solution

We tested the hypothesis that the combination of polymerized bovine hemoglobin (PBHg) with hypertonic saline may be beneficial for the initial management of hemorrhagic shock in 22 mongrel dogs (15 +/- 1 kg) bled to a mean arterial pressure (MAP) of 40 mm Hg in 5 min and maintained at this level for 45 min (shed blood volume approximately 50 ml/kg). Animals were treated with a 4 ml/kg bolus over 4 min of one of the following fluids: whole blood, 7.5% NaCl (HS), 13 g/dl of PBHg, or 7.5% NaCl combined with polymerized bovine hemoglobin (HS-PBHg). No additional intervention was performed, and the animals were followed for 60 min after treatment. PBHg and HS-PBHg produced a sustained, significant increase in MAP. Cardiac output was transiently increased only after HS and HS-PBHg. A partial increase in superior mesenteric artery blood flow was observed, particularly after HS-PBHg. We concluded that small volumes of PBHg alone restore MAP, but not blood flow. The combination of PBHg with hypertonic saline provides improvements in cardiac output and mesenteric blood flow, suggesting a potential benefit for the initial management of major blood loss.     

Hyperosmolar volume replacement in heart surgery]

The ideal solution for use in volume therapy is still a matter of debate. Hypertonic sodium (HS) solutions have been advocated for resuscitation from hemorrhagic shock (small volume resuscitation). As hypertonic fluids may also be of interest in cardiac surgery, the effects of a new HS solution were studied. METHODS. In 90 patients undergoing aorto-coronary bypass grafting studies were performed at three different periods: I (n = 30) after induction of anesthesia (before onset of the operation); II (n = 30) during cardiopulmonary bypass (CPB); III (n = 30) after termination of bypass. During these periods the patients were randomly allocated to one of three groups with 10 patients in each group: group 1 received a new hypertonic solution prepared in hydroxyethyl starch (HES) solution (72 g/l NaCl, 60 g/l HES, 2400 mosmol/l; HS-HES patients), group 2 received a 6% HES solution (200/0.5; HES patients), and group 3 received no volume infusion and served as controls. RESULTS. After the induction of anesthesia, significantly less HS-HES solution (4.5 +/- 0.5 ml/kg) than 6% HES solution (10.1 +/- 1.4 ml/kg) was necessary to double the baseline PCWP. The fluid balance during CPB was negative in the patients who had received HS-HES preoperatively (-0.03 +/- 0.01 ml/kg.min CPB), whereas 6% HES (+0.06 +/- 0.02 ml/kg.min CPB) and control patients (+0.13 +/- 0.03 ml/kg.min CPB) had a positive fluid balance. Both after the induction of anesthesia and after termination of bypass, CI increased more in the HS-HES group than in the HES patients, and it even decreased in the control group. SVR decreased in the HS-HES patients, whereas it increased in the control group. Rapid infusion of HS-HES during CPB was followed by a significant, but short-lasting decrease in MAP (-40 mmHg) and an increase in the oxygenator volume. Pulmonary gas exchange (= paO2) was least compromised in the HS-HES patients; the sodium concentration increased only in the HS-HES patients, but never exceeded 150 mmol/l. DISCUSSION. Cardiac surgery procedures offer a special situation for volume therapy as there is a possibility of deterioration in the macro- and microcirculation before, after, and during the period of CPB. Hemodynamic effects of the new HS-HES solution included an increase in CI and a decrease in SVR, which were not merely transient as has been reported which hypertonic saline solution used alone. It was also observed that HS-HES patients required significantly smaller volumes of fluids, both during CPB and during the early postoperative period. This effect seems to be due to a redistribution of interstitial fluid to the intravascular space, possibly decreasing tissue edema. CONCLUSION. The hypertonic saline HES solution adds a new dimension to volume therapy for cardiac surgery patients. The improvement in hemodynamics was effective and not only transient. Fluid requirements were significantly reduced during as well as after CPB, and pulmonary gas exchange was least compromised in these patients.     

Hemodynamic improvement in hemorrhagic shock by aortic balloon occlusion and hypertonic saline solutions

The initial treatment of uncontrolled hemorrhagic shock from an abdominal source is controversial. The hemodynamic effects of transfemoral diaphragmatic aortic occlusion with a balloon followed by a single bolus of hypertonic saline solutions have been evaluated in 28 dogs. The animals were submitted to pressure-driven hemorrhage for 90 min, according to mean arterial pressure in the abdominal aorta and randomized into four groups, according to the treatment employed at 34 min after hemorrhage. Group 1 dogs (controls) received isotonic NaCl (0.9%, 308 mOsm/l, 4 ml/kg) without aortic occlusion; group 2 underwent aortic occlusion and received isotonic NaCl (0.9%, 308mOsm/l, 4 ml/kg); group 3 were occluded and received hypertonic NaCl (7.5%, 2400mOsm/l, 4 ml/kg); group 4 were occluded and received hypertonic sodium acetate (10.5%, 2400mOsm/l, 4 ml/kg). There were no significant differences between groups at basal measures and also after 30 min of continuous bleeding, when animals presented with severe shock, and significant decreases in mean arterial pressure, cardiac index, systolic index and cardiac filling pressures; the systemic vascular resistance index was increased. Control animals remained in severe shock throughout the experiment and three died. The recovery of mean arterial pressure in aortic-occluded dogs given isotonic NaCl was associated with a marked increase in systemic vascular resistance index, without improvements in cardiac index, systolic index and cardiac filling pressures. In occluded dogs given hypertonic NaCl and NaAc the mean arterial pressure recovery lasted longer, with lower increases in systemic vascular resistance index, while the cardiac index, systolic index and cardiac filling pressures showed a marked albeit transient increase. Injection of hypertonic saline following aortic occlusion produced significantly better hemodynamic profiles and should be seriously considered for the first treatment in severe uncontrolled hemorrhagic shock from an abdominal vascular source.     

Combined hemorrhagic shock and head injury: effects of hypertonic saline (7.5%) resuscitation

Hypertonic saline resuscitation was compared to isotonic fluid resuscitation in a large animal model combining hemorrhagic shock with head injury. Sheep were subjected to a freeze injury of one cerebral hemisphere as well as 2 hours of hypotension at a mean arterial pressure (MAP) of 40 mm Hg. Resuscitation was then carried out (MAP = 80 mm Hg) for 1 hour with either lactated Ringer's (LR, n = 6) or 7.5% hypertonic saline (HS, n = 6). Hemodynamic parameters and intracranial pressure (ICP) were followed. At the end of resuscitation brain water content was determined in injured and uninjured hemispheres. No differences were detected in cardiovascular parameters; however, ICPs were lower in animals resuscitated with HS (4.2 +/- 1.5 mm Hg) compared to LR (15.2 +/- 2.2 mm Hg, p less than 0.05). Additionally, brain water content (ml H2O/gm dry weight) in uninjured brain hemispheres was lower after HS resuscitation (HS = 3.3 +/- 0.1; LR = 4.0 +/- 0.1; p less than 0.05). No differences were detected in the injured hemispheres. We conclude that hypertonic saline abolishes increases in ICP seen during resuscitation in a model combining hemorrhagic shock with brain injury by dehydrating areas where the blood-brain barrier is still intact. Hypertonic saline may prove useful in the early management of multiple trauma patients.     

Effectiveness of hypertonic saline-dextran 70 for initial fluid resuscitation of major burns.

Small-volume resuscitation (4 ml/kg) with hypertonic saline-dextran (HSD) has been shown effective in hemorrhagic shock. In the present study the effectiveness of an initial 4 ml/kg bolus infusion of HSD on cardiovascular function and fluid resuscitation requirements after a major burn injury was evaluated in anesthetized sheep following a 40% BSA scald burn. One hour after injury resuscitation was initiated by a rapid intravenous bolus infusion (4 ml/kg) of either hypertonic saline-dextran (7.5% NaCl in 6% dextran 70) (HSD) or the same volume of normal (isotonic) saline (NS). Lactated Ringer's was later infused as needed to maintain cardiac output at 90% of baseline. HSD rapidly and effectively restored cardiac output and mean arterial pressure significantly better than the same volume of NS. Hemodynamic improvement by HSD was short lived, and need for further fluid therapy was only marginally delayed (HSD 38 +/- 8 min, NS 20 +/- 3 min; p = 0.06) (mean +/- SEM). The total requirements for fluid therapy during the first 6 hr postburn were not reduced by the initial HSD bolus (HSD 3,145 +/- 605 ml, NS 2,905 +/- 495 ml; n.s.), nor was skin edema formation reduced. We conclude that in anesthetized sheep HSD resuscitation was only transiently effective in treating burn shock. This may be attributed to the sustained increase in vascular permeability and continued plasma leak following thermal injury.     

Cerebral hemodynamic effects of fluid resuscitation in the presence of an experimental intracranial mass

We addressed the impact on intracranial pressure (ICP) of posthemorrhage fluid resuscitation with a protocol in which additional fluid was infused to maintain a stable cardiac output after an initial bolus of fluid was infused. Anesthetized, mechanically ventilated mongrel dogs (n = 27) underwent a 30-minute interval of hemorrhagic shock (mean arterial pressure = 55 mm Hg) during which inflation of a subdural balloon maintained ICP at 15 mm Hg. After shock, animals were resuscitated with one of four randomly assigned fluids: (1) slightly hypotonic crystalloid (Na+, 125 mEq.L-1; designated Na-125); (2) hypertonic crystalloid (Na+, 250 mEq.L-1; designated Na-250); (3) slightly hypotonic crystalloid plus 10% pentastarch (Na-125P); or (4) hypertonic crystalloid plus 10% pentastarch (Na-250P). Supplemental fluid was administered as needed to maintain cardiac output comparable to baseline values. ICP increased progressively in all fluid groups during resuscitation. Cerebral blood flow, measured by the cerebral venous outflow method, increased immediately after resuscitation and then declined steadily over time in all groups. Fluids containing pentastarch maintained hemodynamic stability with minimal supplementation throughout most of the postresuscitation period, compared with crystalloid alone, which required substantial additional volume. If decreased intracranial compliance and hemorrhage are combined, ongoing resuscitation is associated with significantly increased ICP and significantly decreased cerebral blood flow, independent of the tonicity and oncotic pressure of the infused fluid.     

高渗氯化钠羟乙基淀粉注射液输注对急性颅内高压伴失血性休克犬脑组织病理学及氧自由基的影响

目的 观察高渗氯化钠羟乙基淀粉40注射液(HSH)在犬急性颅内高压伴失血性休克模型中恢复循环血容量、减轻脑组织水肿和降低脑组织氧自由基含量的作用.方法 健康杂种犬20只,采用硬膜外球囊注水和动脉放血的方法复制急性颅内高压伴失血性休克模型.动物随机分为羟乙基淀粉溶液组(HES组),乳酸盐林格液组(RL组),7.5%氯化钠溶液组(HS组)和高渗氯化钠羟乙基淀粉40注射液组(HSH组),在休克后1 h分别输入相应液体.监测平均动脉压(MAP)、中心静脉压(CVP)、心率(HR)、颅内压(ICP),检测脑组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力,脑组织标本行病理学检查.结果 复苏后4组液体均能有效地升高MAP(P<0.05),但HES组和RL组的ICP上升明显(P<0.05),复苏后2 h,HS组的MAP开始下降(P<0.05).至复苏后4 h,仅HSH组能维持理想的MAP及较低的ICP,HSH组脑组织氧自由基含量较其他组明显减少(P<0.05).病理学检查显示复苏后4 h,HSH组的脑组织损伤较其他组轻.结论 高渗氯化钠羟乙基淀粉40注射液可有效地复苏失血性休克,降低ICP及氧自由基的生成,减轻脑组织缺血/再灌注的损伤.